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Vascular Pathology and Trajectories of Late-Life Major Depressive Disorder in Secondary Psychiatric Care.

ABSTRACT: OBJECTIVE:To examine 5-year trajectories of psychiatrist-treated late-life major depressive disorder (MDD), and evaluate whether previous vascular pathology is associated with more severe trajectories of late-life MDD. METHODS:Data were obtained from nationally representative civil, psychiatric, hospital, and prescription registers in Denmark. The sample included 11,092 older adults (?60 years) who received their first diagnosis of MDD in a psychiatric facility in Denmark between 2000 and 2007. Trajectories of inpatient or outpatient contact at psychiatric hospitals for MDD over the 5-year period following index MDD diagnosis were modeled using latent class growth analysis. Measures of vascular disease (stroke, heart disease, vascular dementia) and vascular risk factors (hypertension, diabetes) were defined based on medication prescriptions and hospital-based diagnoses. Other predictors included demographic characteristics and characteristics of the index MDD diagnosis. RESULTS:The final model included 4 trajectories with consistently low (66% of the sample), high decreasing (19%), consistently high (9%), and moderate fluctuating (6%) probabilities of contact at a psychiatric hospital for MDD during the 5-year period following the index MDD diagnosis. We found no significant associations between any form of vascular pathology and trajectory class membership. Relative to the consistently low class, older age, greater severity and >12 months of prior antidepressant medication use predicted membership in the other three classes. CONCLUSIONS:A notable proportion (34%) of individuals diagnosed with MDD in late-life require secondary psychiatric treatment for extended time periods. We did not find evidence that vascular pathology predicts hospital contact trajectories in secondary-treated late-life MDD.

SUBMITTER: Musliner KL

PROVIDER: S-EPMC5775925 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature

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Vascular Pathology and Trajectories of Late-Life Major Depressive Disorder in Secondary Psychiatric Care.

Musliner Katherine L KL Zandi Peter P PP Liu Xiaoqin X Laursen Thomas M TM Munk-Olsen Trine T Mortensen Preben B PB Eaton William W WW

The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry 20170712 3

<h4>Objective</h4>To examine 5-year trajectories of psychiatrist-treated late-life major depressive disorder (MDD), and evaluate whether previous vascular pathology is associated with more severe trajectories of late-life MDD.<h4>Methods</h4>Data were obtained from nationally representative civil, psychiatric, hospital, and prescription registers in Denmark. The sample included 11,092 older adults (≥60 years) who received their first diagnosis of MDD in a psychiatric facility in Denmark between ...[more]

PMID: 28807498

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Project description:Background: Major Depressive Disorder (MDD) is a moderately heritable disorder with a high lifetime prevalence. At present, laboratory blood tests to support MDD diagnosis are not available. Methods: We used a classifier approach on blood gene expression profiles of a unique set of non-medicated subjects (MDD patients and controls) to select genes of which expression is predictive for disease status. To reveal blood gene expression changes related to MDD disease, we applied a powerful ex vivo stimulus to the blood, i.e. incubation with lipopolysaccharide (LPS; 10 ng/ml blood). Results: Based on LPS-stimulated blood gene expression using whole-genome microarrays in 42 subjects (primary cohort; 21 MDD patients (mean age 42.3 years), 21 healthy controls (mean age 41.9 years)), we identified a set of genes (CAPRIN1, CLEC4A, KRT23, MLC1, PLSCR1, PROK2, ZBTB16) that serves as a molecular signature of MDD. These findings were validated for the primary cohort using an independent quantitative PCR method (P = 0.007). The difference between depressive patients and controls was confirmed (P = 0.019) in a replication cohort of 13 patients with MDD (mean age 42.8 years) and 14 controls (mean age 45.6 years). The MDD-signature score comprised of expression levels of 7 genes could discriminate depressive patients from controls with sensitivity of 76.9% and specificity of 71.8%. Conclusions: We show for the first time that molecular analysis of stimulated blood cells can be used as an endophenotype for MDD diagnosis, which is a milestone in establishing biomarkers for neuropsychiatric disorders with moderate heritability in general. Our results may provide a new entry point for following and predicting treatment outcome, as well as prediction of severity and recurrence of MDD. In total, 33 MDD patients and 34 healthy controls were analyzed using basal gene expression in whole blood, and gene expression from whole blood that was stimulated with LPS for 5-6 h, using microarrays. Patients were arbitrarily selected from all patients to serve as primary cohort (nMDD = 21 (MDD01-MDD21); nControls = 21 (Con01-Con21)), or replication cohort (nMDD = 12 (MDD22-MDD35); nControls = 13 (Con22-Con37)) using microarrays. This submission does not include Samples CON21_LPS or CON30_LPS.

Project description:BackgroundAlthough electroconvulsive therapy (ECT) is an effective treatment for depression, ECT cognitive impairment remains a major concern. The neurobiological underpinnings and mechanisms underlying ECT antidepressant and cognitive impairment effects remain unknown. This investigation aims to identify ECT antidepressant-response and cognitive-impairment multimodal brain networks and assesses whether they are associated with the ECT-induced electric field (E-field) with an optimal pulse amplitude estimation.MethodsA single site clinical trial focused on amplitude (600, 700, and 800 mA) included longitudinal multimodal imaging and clinical and cognitive assessments completed before and immediately after the ECT series (n = 54) for late-life depression. Another two independent validation cohorts (n = 84, n = 260) were included. Symptom and cognition were used as references to supervise fMRI and sMRI fusion to identify ECT antidepressant-response and cognitive-impairment multimodal brain networks. Correlations between ECT-induced E-field within these two networks and clinical and cognitive outcomes were calculated. An optimal pulse amplitude was estimated based on E-field within antidepressant-response and cognitive-impairment networks.ResultsDecreased function in the superior orbitofrontal cortex and caudate accompanied with increased volume in medial temporal cortex showed covarying functional and structural alterations in both antidepressant-response and cognitive-impairment networks. Volume increases in the hippocampal complex and thalamus were antidepressant-response specific, and functional decreases in the amygdala and hippocampal complex were cognitive-impairment specific, which were validated in two independent datasets. The E-field within these two networks showed an inverse relationship with HDRS reduction and cognitive impairment. The optimal E-filed range as [92.7-113.9] V/m was estimated to maximize antidepressant outcomes without compromising cognitive safety.ConclusionsThe large degree of overlap between antidepressant-response and cognitive-impairment networks challenges parameter development focused on precise E-field dosing with new electrode placements. The determination of the optimal individualized ECT amplitude within the antidepressant and cognitive networks may improve the treatment benefit-risk ratio.Trial registrationClinicalTrials.gov Identifier: NCT02999269.

Dataset Information

Vascular Pathology and Trajectories of Late-Life Major Depressive Disorder in Secondary Psychiatric Care.

Publications

Vascular Pathology and Trajectories of Late-Life Major Depressive Disorder in Secondary Psychiatric Care.

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